Magnolol protects against ischemic-reperfusion brain damage following oxygen-glucose deprivation and transient focal cerebral ischemia

研究成果: Article

2 引文 (Scopus)

摘要

In the present study, the neuroprotective potential of magnolol against ischemia-reperfusion brain injury was examined via in vivo and in vitro experiments. Magnolol exhibited strong radical scavenging and antioxidant activity, and significantly inhibited the production of interleukin-6, tumor necrosis factor-A and nitrite/nitrate (NOX) in lipopolysaccharide-stimulated BV2 and RAW 264.7 cells when applied at concentrations of 10 and 50 μM, respectively. Magnolol (100 μM) also significantly attenuated oxygen-glucose deprivation-induced damage in neonatal rat hippocampal slice cultures, when administered up to 4 h following the insult. In a rat model of stable ischemia, compared with a vehicle-Treated ischemic control, pretreatment with magnolol (0.01-1 mg/kg, intravenously) significantly reduced brain infarction following ischemic stroke, and post-Treatment with magnolol (1 mg/kg) remained effective and significantly reduced infarction when administered 2 h following the onset of ischemia. Additionally, magnolol (0.3 and 1 mg/kg) significantly reduced the accumulation of superoxide anions at the border zones of infarction and reduced oxidative damage in the ischemic brain. This was assessed by measuring the levels of NOX, malondialdehyde and myeloperoxidase, the ratio of glutathione/oxidized glutathione and the immunoreactions of 8-hydroxy-2'-deoxyguanosine and 4-hydroxynonenal. Thus, magnolol was revealed to protect against ischemia-reperfusion brain damage. This may be partly attributed to its antioxidant, radical scavenging andanti-inflammatory effects.

原文English
頁(從 - 到)2252-2262
頁數11
期刊International journal of molecular medicine
41
發行號4
DOIs
出版狀態Published - 2018 四月 1

指紋

Transient Ischemic Attack
Reperfusion Injury
Oxygen
Glucose
Brain
Infarction
Ischemia
Antioxidants
Brain Infarction
Glutathione Disulfide
Nitrites
magnolol
Brain Ischemia
Malondialdehyde
Superoxides
Nitrates
Brain Injuries
Peroxidase
Glutathione
Lipopolysaccharides

All Science Journal Classification (ASJC) codes

  • Genetics

引用此文

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title = "Magnolol protects against ischemic-reperfusion brain damage following oxygen-glucose deprivation and transient focal cerebral ischemia",
abstract = "In the present study, the neuroprotective potential of magnolol against ischemia-reperfusion brain injury was examined via in vivo and in vitro experiments. Magnolol exhibited strong radical scavenging and antioxidant activity, and significantly inhibited the production of interleukin-6, tumor necrosis factor-A and nitrite/nitrate (NOX) in lipopolysaccharide-stimulated BV2 and RAW 264.7 cells when applied at concentrations of 10 and 50 μM, respectively. Magnolol (100 μM) also significantly attenuated oxygen-glucose deprivation-induced damage in neonatal rat hippocampal slice cultures, when administered up to 4 h following the insult. In a rat model of stable ischemia, compared with a vehicle-Treated ischemic control, pretreatment with magnolol (0.01-1 mg/kg, intravenously) significantly reduced brain infarction following ischemic stroke, and post-Treatment with magnolol (1 mg/kg) remained effective and significantly reduced infarction when administered 2 h following the onset of ischemia. Additionally, magnolol (0.3 and 1 mg/kg) significantly reduced the accumulation of superoxide anions at the border zones of infarction and reduced oxidative damage in the ischemic brain. This was assessed by measuring the levels of NOX, malondialdehyde and myeloperoxidase, the ratio of glutathione/oxidized glutathione and the immunoreactions of 8-hydroxy-2'-deoxyguanosine and 4-hydroxynonenal. Thus, magnolol was revealed to protect against ischemia-reperfusion brain damage. This may be partly attributed to its antioxidant, radical scavenging andanti-inflammatory effects.",
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T1 - Magnolol protects against ischemic-reperfusion brain damage following oxygen-glucose deprivation and transient focal cerebral ischemia

AU - Huang, Sheng Yang

AU - Tai, Shih-Huang

AU - Chang, Che-Chao

AU - Tu, Yi-Fang

AU - Chang, Chih-Han

AU - Lee, E-Jian

PY - 2018/4/1

Y1 - 2018/4/1

N2 - In the present study, the neuroprotective potential of magnolol against ischemia-reperfusion brain injury was examined via in vivo and in vitro experiments. Magnolol exhibited strong radical scavenging and antioxidant activity, and significantly inhibited the production of interleukin-6, tumor necrosis factor-A and nitrite/nitrate (NOX) in lipopolysaccharide-stimulated BV2 and RAW 264.7 cells when applied at concentrations of 10 and 50 μM, respectively. Magnolol (100 μM) also significantly attenuated oxygen-glucose deprivation-induced damage in neonatal rat hippocampal slice cultures, when administered up to 4 h following the insult. In a rat model of stable ischemia, compared with a vehicle-Treated ischemic control, pretreatment with magnolol (0.01-1 mg/kg, intravenously) significantly reduced brain infarction following ischemic stroke, and post-Treatment with magnolol (1 mg/kg) remained effective and significantly reduced infarction when administered 2 h following the onset of ischemia. Additionally, magnolol (0.3 and 1 mg/kg) significantly reduced the accumulation of superoxide anions at the border zones of infarction and reduced oxidative damage in the ischemic brain. This was assessed by measuring the levels of NOX, malondialdehyde and myeloperoxidase, the ratio of glutathione/oxidized glutathione and the immunoreactions of 8-hydroxy-2'-deoxyguanosine and 4-hydroxynonenal. Thus, magnolol was revealed to protect against ischemia-reperfusion brain damage. This may be partly attributed to its antioxidant, radical scavenging andanti-inflammatory effects.

AB - In the present study, the neuroprotective potential of magnolol against ischemia-reperfusion brain injury was examined via in vivo and in vitro experiments. Magnolol exhibited strong radical scavenging and antioxidant activity, and significantly inhibited the production of interleukin-6, tumor necrosis factor-A and nitrite/nitrate (NOX) in lipopolysaccharide-stimulated BV2 and RAW 264.7 cells when applied at concentrations of 10 and 50 μM, respectively. Magnolol (100 μM) also significantly attenuated oxygen-glucose deprivation-induced damage in neonatal rat hippocampal slice cultures, when administered up to 4 h following the insult. In a rat model of stable ischemia, compared with a vehicle-Treated ischemic control, pretreatment with magnolol (0.01-1 mg/kg, intravenously) significantly reduced brain infarction following ischemic stroke, and post-Treatment with magnolol (1 mg/kg) remained effective and significantly reduced infarction when administered 2 h following the onset of ischemia. Additionally, magnolol (0.3 and 1 mg/kg) significantly reduced the accumulation of superoxide anions at the border zones of infarction and reduced oxidative damage in the ischemic brain. This was assessed by measuring the levels of NOX, malondialdehyde and myeloperoxidase, the ratio of glutathione/oxidized glutathione and the immunoreactions of 8-hydroxy-2'-deoxyguanosine and 4-hydroxynonenal. Thus, magnolol was revealed to protect against ischemia-reperfusion brain damage. This may be partly attributed to its antioxidant, radical scavenging andanti-inflammatory effects.

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